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Vol 17, No 2 (2011)
Research paper
Published online: 2011-07-04

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Vascular endothelial growth factor and its receptors in the varicose vein wall

Radosław Kowalewski, Andrzej Małkowski, Krzysztof Sobolewski, Marek Gacko
Acta Angiologica 2011;17(2):141-149.

Abstract

Background. Disturbances in the regulation of vessel wall homeostasis are a potential factor initiating varicose vein development. Vascular endothelial growth factor A (VEGF-A) may play a hypothetic role in this process. The aim of the study was to evaluate mRNA expression and protein content of VEGF-A and its receptors (VEGF R1, VEGF R2) in varicose veins and varicose veins complicated by thrombophlebitis.
Material and methods. Walls of varicose veins and varicose veins complicated by thrombophlebitis were the studied material. Walls of normal saphenous veins, which were harvested from patients with chronic limb ischaemia undergoing infrainguinal by-pass grafting, were the control material. The RT-PCR method was employed to assess mRNA expression of VEGF-A and its receptors, whereas the ELISA method was used to evaluate contents of VEGF-A and its receptors.
Results. VEGF-A and VEGF R2 mRNA expression is increased, whereas VEGF R1 mRNA expression is unchanged in the wall of varicose veins in comparison with the wall of normal ones. VEGF-A and VEGF R1 mRNA expression is increased in the wall of varicose veins complicated by thrombophlebitis in comparison with walls of normal and varicose veins. VEGF R2 mRNA expression is also increased in the wall of varicose veins complicated by thrombophlebitis in comparison with control veins, but it is comparable to that in the wall of varicose veins. Changes in mRNA expression are correlated with appropriate changes in protein contents of VEGF-A, VEGF R1, and VEGF R2.
Conclusions. The demonstrated changes in mRNA expression, as well as in the contents of VEGF-A, VEGF R1, and VEGF R2, in the wall of varicose veins may be accepted as one of the reasons for the clinical symptoms of the disease and can predispose to its progression.
Acta Angiol 2011; 17, 2: 141–149

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